J. Soška

Mutagenic activities of simple nitrofuran derivatives. I. Comparison of related compounds in the phage inductest, chloroplast-bleaching and bacterial-repair and mutagenicity tests.

Several simple furan and nitrofuran compounds were tested for mutagenicity and related biological activities, in the Ames test, the bacterial repair test, the prophage-induction test and the chloroplast-bleaching test. Only those compounds having the nitro-group were found to be active in the test. If the nitro-group was in the beta instead of the alpha position, the mutagenic activity was much reduced (0.3 revertants per nanomole, the other simple nitrofurans producing 5-15 reversions per nanomole, as did 5-nitrofuran and 5,2-dinitrofuran). The vinyl-group-containing compound, 5-nitro-2-furylacrylic acid, was by one decadic order more effective both in the Ames test and in the prophage-induction test. In the repair tests all nitrofurans displayed a much higher dependence on the recA-repair system than on the uvrA system. For 2 compounds, the dinitrofuran and, especially, the 5-nitrofuraldehyde, the urA cells were even less sensitive than the wild-type cells.

Repression of ant synthesis early in the lytic cycle of phage P22.

SummaryUsing SDS-polyacrylamide gel electrophoresis to study the early expression of P22 genes we show that early expression of the ant-gene (imm I region) is turned off after 6–8 min, independent of the ‘late’ acting mnt-repressor. A semi-clear mutant called cir5 is defective for this early ant turn-off. The mutation cir5 maps in the imm I region of P22 between genes mnt and ant. P22 cir5 mutants are defective for a repressor which acts in trans to regulate early ant synthesis. There appears to be no absolute requirement of the cir5 allele for the establishment of lysogeny. The overproduction of ant in the P22 cir5 mutant leads to a marked increase in abortive infections, killing the infected cells. The cir5-phenotype can be suppressed by an ant- mutation.

Inhibition of thymine synthesis inLactobacillus acidophilus R-26 by deoxyadenosine-5′-monophosphate

Growth ofLactobacillus acidophilus was inhibited in the presence of deoxyadenosine-5′-monophosphate (dAMP). The other purine deoxyribonucleotides and -sides were only weak inhibitors, and pyrimidine deoxyribotides and -sides were inactive. dAMP did not act as an inhibitor if thymine, thymidine, or 5-methyldeoxycytidine-5′-monophosphate was present in the medium. The inhibition by dAMP was counteracted by increasing concentrations of deoxyuridine, deoxyuridine-5′-monophosphate and, to some extent, adenosine-5′-monophosphate. The effect of these substances was proportional to their concentration and competitive in character. The results support the assumption that dAMP inhibits the synthesis of thymine. Mutants ofL. acidophilus resistant to inhibition by dAMP were found.

Genome modifications in protoplast-derived tobacco plants: Contents of repetitive DNA sequences

Plasticity of the tobacco genome was studied by testing the DNAs of protoplast-derived regenerants with three different repetitive DNA sequences by the method of quantitative DNA/DNA hybridizations. A large population of 91 regenerants belonging to 35 different protoclones was analysed and a high degree of heterogeneity in the contents of the different DNA repeats was detected. The contents of middle repetitive sequences of two types were more stable or changed in the same direction, while the highly repetitive sequence varied independently and displayed a significant reduction in comparison with the two other sequences. Comparing the variation within the subpopulations of plants of the same clonal origin and the variation among the protoclones led to a conclusion that the pre-existing DNA variability in the starting plant material and/or thein vitro stress during the very early stages of protoclone regeneration played a decisive role in the formation of modified genomes in regenerants.

The immI region of Salmonella phage P22

SummarySalmonella phage mutants P22 cir4-1, P22 cir5-1 and P22 cir6-1 at 37°C form more or less clear plaques. The mutants complement each other and clear mutations of the immC region (Prell et al. 1983). The mutants exhibit a strongly reduced frequency of lysogenisation, but form stable prophages. The low frequency of lysogenisation of P22 cir5-1 and of P22 cir6-1 is suppressed by an additional ant- mutation. Similarly, about 50% of turbid plaque revertants of both mutants carry ant- suppressor mutations. This suggests interference by the cir5-1 and cir6-1 mutations with the expression of gene ant. In contrast, the cir4-1 mutation seems not to interfere with ant expression, the latent periods of P22 cir4-1 and P22 cir5-1 are reduced and extended, respectively. The geneticly related Salmonella phage L carries a gene able to complement P22 cir4-1.

The kinetics of the requirement for X gene product in bacteriophage P22

SummaryThe kinetic study of the requirement for X gene product showed that the average burst size of the P22 phage depended on the length of the permissive interval in which the X function was expressed. Results of the temperature shift experiments with the clear plaque recombinants tsX c25and ts 25.1 c25gave a complicated pattern of the phage yield response.It is concluded that X gene product, besides the control function in the initiation of the phage development, is involved directly or indirectly in the control of late functions and is required throughout the entire period of the phage development.